Effect of t-butylhydroperoxide on Na+/-dependent glutamate uptake in rabbit brain synaptosome.
- Author:
Hyun Je LEE
1
;
Yong Keun KIM
Author Information
1. Department of Physiology, College of Medicine, Pusan National University, Pusan 602-739, Korea.
- Publication Type:Original Article
- Keywords:
t-butylhydroperoxide;
Glutamate uptake;
Lipid peroxidation;
Na+-K+-ATPase activity;
Rabbit brain synaptosomes
- MeSH:
Antioxidants;
Brain*;
Butylated Hydroxyanisole;
Carrier Proteins;
Cerebral Cortex;
Chelating Agents;
Diltiazem;
Glutamic Acid*;
Iron;
Lipid Peroxidation;
Membranes;
Phenol;
Synaptosomes*;
tert-Butylhydroperoxide*
- From:The Korean Journal of Physiology and Pharmacology
1997;1(4):367-376
- CountryRepublic of Korea
- Language:English
-
Abstract:
The effect of an organic peroxide, t-butylhydroperoxide (t-BHP), on glutamate uptake was studied in synaptosomes prepared from cerebral cortex. t-BHP inhibited the Na+/-dependent glutamate uptake with no change in the Na+/-independent uptake. This effect of t-BHP was not altered by addition of Ca2+ channel blockers (verapamil, diltiazem and nifedipine) or PLA2 inhibitors (dibucaine, butacaine and quinacrine). However, the effect was prevented by iron chelators (deferoxamine and phenanthroline) and phenolic antioxidants (N,N'-diphenyl-phenylenediamine, butylated hydroxyanisole, and butylated hydroxytoluene). At low concentrations (< 1.0 mM), t-BHP inhibited glutamate uptake without altering lipid peroxidation. Moreover, a large increase in lipid peroxidation by ascorbate/Fe2+ was not accompanied by an inhibition of glutamate uptake. The impairment of glutamate uptake by t-BHP was not intimately related to the change in Na+/-K+/-ATPase activity. These results suggest that inhibition of glutamate uptake by t-BHP is not totally mediated by peroxidation of membrane lipid, but is associated with direct interactions of glutamate transport proteins with t-BHP metabolites. The Ca2+ influx through Ca2+ channel or PLA2 activation may not be involved in the t-BHP inhibition of glutamate transport.
